Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle

Abstract

Introduction Loss of mitochondrial competency is associated with several chronic illnesses. Therefore, strategies that maintain or increase mitochondrial function will likely be of benefit in a number of clinical settings. Endurance exercise has long been known to increase mitochondrial function in skeletal muscle. Comparatively little is known regarding the impact of resistance exercise training on skeletal muscle mitochondrial respiratory function. Purpose The purpose of the current study was to determine the impact of chronic resistance training on skeletal muscle mitochondrial respiratory capacity and function. Methods Here, we studied the impact of a 12-week resistance exercise training program on skeletal muscle mitochondrial function in eleven young healthy men. Muscle biopsies were collected before and after the 12-week training program and mitochondrial respiratory capacity determined in permeabilized myofibers by high-resolution respirometry. Results Resistance exercise training increased lean body mass and quadriceps muscle strength by 4 and 15%, respectively (P<0.001). Coupled mitochondria respiration supported by complex I, and complex I and II substrates, increased by 2- and 1.4-fold, respectively (P<0.01). The ratio of coupled complex I supported respiration to maximal respiration increased with resistance exercise training (P<0.05), as did complex I protein abundance (P<0.05), while the substrate control ratio for succinate was reduced after resistance exercise training (P<0.001). Transcripts responsible for proteins critical to electron transfer and NAD+ production increased with training (P<0.05), while transcripts involved in mitochondrial biogenesis were unaltered. Conclusion Collectively, 12-weeks of resistance exercise training resulted in qualitative and quantitative changes in skeletal muscle mitochondrial respiration. This adaptation occurs with modest changes in mitochondrial proteins and transcript expression. Resistance exercise training appears to be a means to augment the respiratory capacity and intrinsic function of skeletal muscle mitochondria.

Post-absorptive muscle protein turnover affects resistance training hypertrophy

“…After the DXA scan, ultrasound (Phillips HDI 5000) of the VL muscle was conducted while the participants remained supine, as previously described (Porter et al 2015). Briefly, several B-Mode real-time images of the VL were taken in the mid-sagittal position at 50% (mid-belly) and 25% (distal) of the femur length (from the anterior superior iliac spine to the superior border of the patella).…”

“…Peak torque and power of the knee extensors and knee flexors of the non-biopsied leg were subsequently determined by dynamometry (Biodex Medical, Shirley, NY), as previously conducted (Porter et al 2015). …”

“…Participants were allowed to maintain their recreational physical activity but instructed not to do any other strength training outside the study. RET was performed at an intensity of 60-80% of 1-RM strength and consisted of 3-4 sets of 8-10 repetitions performed to failure for each exercise, as previously conducted (Porter et al 2015). 1-RM strength was directly tested on the chest press, leg press, and knee extension.…”

Mitochondria Initiate and Regulate Sarcopenia

“…Both endurance and resistance exercise have been associated with elevated mitochondrial biogenesis (93, 109). Relative mitochondrial activity corresponds with fractional protein synthesis rates, because many proteins complete their translation at mitochondria (84).…”

A Ketogenic Diet in Rodents Elicits Improved Mitochondrial Adaptations in Response to Resistance Exercise Training Compared to an Isocaloric Western Diet

“…Although many of these disorders are also associated with mitochondrial dysfunction (Kelley et al, 2002; Ritov et al, 2005; Lin and Beal, 2006), the majority of previous research regarding mitochondrial function and a KD has been centered around the effects of a KD on neuronal tissue in the brain. While mitochondria are a diverse organelle capable of responding to a multitude of metabolic stressors such as aerobic and/or resistance exercise and caloric restriction (Gredilla et al, 2001; Menshikova et al, 2006; Salvadego et al, 2013; Porter et al, 2015), differing metabolic profiles exist between the brain and skeletal muscle due to the blood brain barrier (Pardridge, 1983). Currently the effects of a KD on skeletal muscle mitochondria are not well understood.…”