ObjectiveThe purpose of this study was to compare the acute physiological, perceptual, and enjoyment responses between bodyweight high-intensity interval exercise (BW-HIIE) and treadmill running high-intensity interval exercise HIIE (RUN-HIIE).MethodsTwelve adults [age: 29.5 ± 5.3 years; weight: 70.9 ± 15.0 kg; height: 167.9 ± 8.9 cm; peak oxygen consumption (VO2 peak): 48.7 ± 6.5 ml min−1·kg−1] performed both RUN-HIIE and BW-HIIE. RUN-HIIE consisted of two sets of 5, 60-s (s) run intervals at 100% of the speed achieved during VO2 peak testing followed by 60s of walking at 4.02 km/h. BW-HIIE consisted of two sets of 5, 60s ‘all-out’ effort calisthenic exercises followed by 60s of marching in place at 100 steps per minute. Oxygen consumption (VO2), blood lactate (Blac), heart rate (HR), and rating of perceived exertion (RPE) were measured during exercise. Physical activity enjoyment (PACES) was assessed post-exercise. Creatine Kinase (CK) was measured before exercise and 48-h post-exercise. Muscle soreness was assessed before exercise, post-exercise, and 48-h post-exercise.ResultsOxygen consumption relative to VO2 peak was higher (p < 0.001) during RUN-HIIE (88 ± 3%) compared to BW-HIIE (77 ± 4%). HR relative to HRpeak was higher (p = 0.002) for RUN-HIIE (93 ± 1%) compared to BW-HIIE (88 ± 2%). Blac was higher (p < 0.001) after BW-HIIE (11.2 ± 3.2 mmol/l) compared to RUN-HIIE (6.9 ± 2.0 mmol/l). Average RPE achieved was higher (p = 0.003) during BW-HIIE (16 ± 2) than RUN-HIIE (14 ± 2). PACES was similar for RUN-HIIE and BW-HIIE (p > 0.05). No differences (p > 0.05) in CK were observed between RUN-HIIE and BW-HIIE.ConclusionOur results indicate ‘all-out’ calisthenic exercise can elicit vigorous cardiorespiratory, Blac, and RPE responses. Implementing this style of exercise into training requires minimal space, no equipment, and may elicit cardiometabolic adaptations seen with traditional forms of high-intensity exercise.

Conditions characterized by muscle wasting such as cachexia and sarcopenia are devastating at the individual level, and they place a profound burden on public health. Evidence suggests that inflammation is likely a mechanistic contributor to the pathogenesis of these conditions. One specific molecule, lipopolysaccharide, has gained attention due to its role in initiating inflammation. Toll-like receptor-4 is the primary receptor for lipopolysaccharide and has been shown to be implicit in the downstream proinflammatory response associated with lipopolysaccharide. Importantly, Toll-like receptor-4 is expressed on various cell types throughout the human body such as leukocytes and skeletal muscle fibers and may have site-specific effects that contribute to muscle wasting conditions based on the location in which activation occurs. Accordingly, reducing proinflammatory signaling at these locations may be an effective strategy at mitigating muscle wasting. Regular exercise training is believed to elicit anti-inflammatory adaptations, but the mechanisms by which this occurs are yet to be fully understood. Understanding the mechanisms by which Toll-like receptor-4 activation contributes to muscle wasting and how exercise affects this, may allow for the development of a non-pharmacological therapeutic intervention. Therefore, in this review, we summarize the current understanding of the lipopolysaccharide/Toll-like receptor-4 axis in leukocytes and skeletal muscle fibers on the pathogenesis of muscle wasting conditions and we critically examine the current evidence regarding the effects of exercise on this axis.

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Generally, skeletal muscle adaptations to exercise are perceived through a dichotomous lens where the metabolic stress imposed by aerobic training leads to increased mitochondrial adaptations while the mechanical tension from resistance training leads to myofibrillar adaptations. However, there is emerging evidence for cross over between modalities where aerobic training stimulates traditional adaptations to resistance training (e.g., hypertrophy) and resistance training stimulates traditional adaptations to aerobic training (e.g., mitochondrial biogenesis). The latter is the focus of the current review in which we propose high-volume resistance training (i.e., high time under tension) leads to aerobic adaptations such as angiogenesis, mitochondrial biogenesis, and increased oxidative capacity. As time under tension increases, skeletal muscle energy turnover, metabolic stress, and ischemia also increase, which act as signals to activate the peroxisome proliferator-activated receptor gamma coactivator 1-alpha, which is the master regulator of mitochondrial biogenesis. For practical application, the acute stress and chronic adaptations to three specific forms of high-time under tension are also discussed: Slow-tempo, low-intensity resistance training, and drop-set resistance training. These modalities of high-time under tension lead to hallmark adaptations to resistance training such as muscle endurance, hypertrophy, and strength, but little is known about their effect on traditional aerobic training adaptations.

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