Critical power and work-prime account for variability in endurance training adaptations not captured by V̇o2max.

Responses to exercise at a given percentage of one's maximum rate of oxygen consumption (V̇o2max), or percentage of the power associated with V̇o2max during a graded exercise test (i.e., PGXT), vary. The purpose of this study was to determine if differences in critical power (PCRIT, maximum metabolic steady state) and work-prime (W', the amount of work tolerated above steady state) are related to training-induced changes in endurance. PCRIT, W', V̇o2max, and other variables were determined before and after 22 adults completed 8 wk of either moderate-intensity continuous training (MICT) or high-intensity interval training (HIIT) performed at fixed percentages of PGXT. On average, PCRIT increased to a greater extent following HIIT (MICT: 15.7 ± 3.1% vs. HIIT: 27.5 ± 4.3%; P = 0.03), but the magnitude of change varied widely within each group (MICT: 4%-36%, HIIT: 4%-61%). The intensity of the prescribed exercise relative to pretraining PCRIT, not PGXT, accounted for most of the variance in changes to PCRIT in response to a given protocol (R2 = 0.61-0.64; P < 0.01). Although PCRIT and V̇o2max were related before training (R2 = 0.92, P < 0.01), the training-induced change in PCRIT was not significantly related to the change in V̇o2max (R2 = 0.06, P = 0.26). Before training, time-to-failure at PGXT was related to W' (R2 = 0.52; P < 0.01), but not V̇o2max (R2 = 0.13; P = 0.10). Training-induced changes in time-to-failure at the initial PGXT were better captured by the combined changes in W' and PCRIT (R2 = 0.77, P < 0.01), than by the change in V̇o2max (R2 = 0.24; P = 0.02). Differences in PCRIT and W' account for some of the variability in responses to endurance exercise.NEW & NOTEWORTHY As the highest percentage of V̇O2max at which steady state conditions can be achieved, a person's critical power (PCRIT) strongly influences the metabolic strain of a given exercise. In this study we demonstrate that training-induced changes in endurance are more strongly related to the intensity of an exercise training program, relative to PCRIT than relative to V̇o2max. Thus, exercise may be more homogenously and effectively prescribed in relation to PCRIT than traditional factors like V̇o2max.

Localized Heat Therapy Improves Mitochondrial Respiratory Capacity but Not Fatty Acid Oxidation.

AIM: Mild heat stress can improve mitochondrial respiratory capacity in skeletal muscle. However, long-term heat interventions are scarce, and the effects of heat therapy need to be understood in the context of the adaptations which follow the more complex combination of stimuli from exercise training. The purpose of this work was to compare the effects of 6 weeks of localized heat therapy on human skeletal muscle mitochondria to single-leg interval training. METHODS: Thirty-five subjects were assigned to receive sham therapy, short-wave diathermy heat therapy, or single-leg interval exercise training, localized to the quadriceps muscles of the right leg. All interventions took place 3 times per week. Muscle biopsies were performed at baseline, and after 3 and 6 weeks of intervention. Mitochondrial respiratory capacity was assessed on permeabilized muscle fibers via high-resolution respirometry. RESULTS: The primary finding of this work was that heat therapy and exercise training significantly improved mitochondrial respiratory capacity by 24.8 ± 6.2% and 27.9 ± 8.7%, respectively (p < 0.05). Fatty acid oxidation and citrate synthase activity were also increased following exercise training by 29.5 ± 6.8% and 19.0 ± 7.4%, respectively (p < 0.05). However, contrary to our hypothesis, heat therapy did not increase fatty acid oxidation or citrate synthase activity. CONCLUSION: Six weeks of muscle-localized heat therapy significantly improves mitochondrial respiratory capacity, comparable to exercise training. However, unlike exercise, heat does not improve fatty acid oxidation capacity.