The study aim was to compare the predictive validity of the often referenced traditional model of human endurance performance (i.e. oxygen consumption, VO 2 , or power at maximal effort, fatigue threshold values, and indices of exercise efficiency) versus measures of skeletal muscle oxidative potential in relation to endurance cycling performance. We hypothesized that skeletal muscle oxidative potential would more completely explain endurance performance than the traditional model, which has never been collectively verified with cycling. Accordingly, we obtained nine measures of VO 2 or power at maximal efforts, 20 measures reflective of various fatigue threshold values, 14 indices of cycling efficiency, and near-infrared spectroscopy-derived measures reflecting in vivo skeletal muscle oxidative potential. Forward regression modeling identified variable combinations that best explained 25-km time trial time-to-completion (TTC) across a group of trained male participants (n = 24). The time constant for skeletal muscle oxygen consumption recovery, a validated measure of maximal skeletal muscle respiration, explained 92.7% of TTC variance by itself (Adj R 2 = .927, F = 294.2, SEE = 71.2, p < .001). Alternatively, the best complete traditional model of performance, including VO 2max (L·min −1 ), %VO 2max determined by the ventilatory equivalents method, and cycling economy at 50 W, only explained 76.2% of TTC variance (Adj R 2 = .762, F = 25.6, SEE = 128.7,p < .001). These results confirm our hypothesis by demonstrating that maximal rates of skeletal muscle respiration more completely explain cycling endurance performance than even the best combination of traditional variables long postulated to predict human endurance performance.

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Aerobic training remodels the quantity and quality (function per unit) of skeletal muscle mitochondria to promote substrate oxidation, however, there remain key gaps in understanding the underlying mechanisms during initial training adaptations. We used short-term high-intensity interval training (HIIT) to determine changes to mitochondrial respiration and regulatory pathways that occur early in remodeling. Fifteen normal-weight sedentary adults started seven sessions of HIIT over fourteen days and fourteen participants completed the intervention. We collected vastus lateralis biopsies before and 48-hours after HIIT to determine mitochondrial respiration, RNA sequencing, and western blotting for proteins of mitochondrial respiration and degradation via autophagy. HIIT increased respiration per mitochondrial protein for lipid (+23% P=0.020), complex I (+18%, P=0.0015), complex I+II (+14%, P<0.0001) and complex II (+24% P<0.0001). Transcripts that increased with HIIT identified several gene sets of mitochondrial respiration, particularly for complex I, while transcripts that decreased identified pathways of DNA and chromatin remodeling. HIIT lowered protein abundance of autophagy markers for p62 (-19%, P=0.012) and LC3 II/I (-20%, P=0.004) in whole-tissue lysates but not isolated mitochondria. Meal tolerance testing revealed HIIT increased the change in whole-body respiratory exchange ratio and lowered cumulative plasma insulin concentrations. Gene transcripts and respiratory function indicate remodeling of mitochondria within 2 weeks of HIIT. Overall changes are consistent with increased protein quality driving rapid improvements in substrate oxidation.

Individuals who are exposed to an increased risk of experiencing a hemorrhagic insult, such as soldiers and firefighters, are often required to complete intermittent high intensity exercise in the presence of environmental heat stress. In normothermic conditions, increases in heart rate and reductions in vascular resistance can be greater following high intensity interval exercise relative to continuous steady state exercise. These hemodynamic alterations following high intensity interval exercise may reduce the capacity to withstand a hemorrhagic insult. We investigated whether high intensity interval exercise reduces tolerance to a simulated hemorrhagic challenge (lower body negative pressure; LBNP) relative to steady state exercise in heat stressed individuals. Eight healthy participants (Age: 27 ± 5 years; Ht: 179 ± 9 cm; Wt: 78.9 ± 18.7 kg) completed two trials (Steady state and Interval). Participants performed cycling exercise either by alternating between 10 and 88% (Interval) or continuously at 38% (Steady state) of the predetermined maximal aerobic power output whilst wearing a warm water perfused suit until core temperatures increased by 1.40 ± 0.21°C. Participants then underwent progressive LBNP (−20mmHg, −30mmHg, etc.) to pre syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Following exercise and prior to LBNP, mean skin temperatures were similarly elevated from baseline in both trials (from: 32.35 ± 0.42 to 37.95 ± 0.59°C, P < 0.05). Mean arterial pressure was not different between trials prior to LBNP (Interval: 79 ± 6 vs. Steady state: 77 ± 7 mmHg; P = 0.57) and were similarly reduced in both trials at pre syncope (to 63 ± 6 and 62 ± 6 mmHg respectively, both P < 0.05). CSI was lower in the interval trial relative to the steady state trial (280 ± 204 vs. 518 ± 285 mmHg*min, respectively; P = 0.024). In heat stressed individuals, tolerance to a simulated hemorrhagic challenge was reduced following high intensity interval exercise relative to steady state exercise. These findings have implications for individuals who exercise at intermittent high intensities in hot environments and are at increased risk of experiencing a hemorrhagic injury (e.g. soldiers, firefighters and miners). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.