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This study aimed to investigate the effect of 3 different eccentric-only power training volumes on muscle fiber type composition and power performance. Twenty-nine females were assigned into 3 groups and performed 10 weeks of either 3 (low volume), 6 (moderate volume), or 9 (high volume) sets/session of 4 fast-velocity eccentric-only half-squats against 70% of concentric 1-repetition maximum (1RM), followed by 3 maximum countermovement jumps (CMJs) after each set. Half-squat 1RM, CMJ height/power, maximum isometric force, rate of force development (RFD) and muscle fiber cross-sectional area (CSA) were increased in all groups (p = 0.001). Low-volume training induced higher increases in CMJ height/power and early RFD, compared with the moderate- and high-volume training programs (p < 0.001). Significant reductions in type IIx muscle fiber percentages and %CSAs were found after moderate- and high-volume training, with concomitant increases in type IIa fibers (p = 0.001). Significant correlations were found between the changes in type IIa and type IIx percentages, fiber CSA, %CSA, and the changes in performance (r: -0.787 to 0.792; p < 0.05). These results suggest that relatively large eccentric power training volumes may result in detrimental neuromuscular adaptations, minimal changes in early RFD, and a reduction of type IIx muscle fiber percentage. Novelty Low but not high volume of power training maintains type IIx muscle fibers. Early rate of force development increases after a low- or moderate-power training volume, but not after a high-power training volume. Training-induced changes in type IIx muscle fiber percentage is related with changes in early rate of force development.

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Skeletal muscle dysfunction in patients with chronic obstructive pulmonary disease negatively impacts quality of life and survival. Cigarette smoking (CS) is the major risk factor for chronic obstructive pulmonary disease and skeletal muscle dysfunction; however, how CS affects skeletal muscle function remains enigmatic. To examine the impact of CS on skeletal muscle inflammation and regeneration, male BALB/c mice were exposed to CS for 8 weeks before muscle injury was induced by barium chloride injection, and were maintained on the CS protocol for up to 21 days after injury. Barium chloride injection resulted in architectural damage to the tibialis anterior muscle, resulting in a decrease contractile function, which was worsened by CS exposure. CS exposure caused muscle atrophy (reduction in gross weight and myofiber cross-sectional area) and altered fiber type composition (31% reduction of oxidative fibers). Both contractile function and loss in myofiber cross-sectional area by CS exposure gradually recovered over time. Satellite cells are muscle stem cells that confer skeletal muscle the plasticity to adapt to changing demands. CS exposure blunted Pax7+ centralized nuclei within satellite cells and thus prevented the activation of these muscle stem cells. Finally, CS triggered muscle inflammation; in particular, there was an exacerbated recruitment of F4/80+ monocytic cells to the site of injury along with enhanced proinflammatory cytokine expression. In conclusion, CS exposure amplified the local inflammatory response at the site of skeletal muscle injury, and this was associated with impaired satellite cell activation, leading to a worsened muscle injury and contractile function without detectable impacts on the recovery outcomes.

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Muscle atrophy typically is a direct effect of protein degradation induced by a diversity of pathophysiologic states such as disuse, immobilization, denervation, aging, sepsis, cachexia, glucocorticoid treatment, hereditary muscular disorders, cancer, diabetes and obesity, kidney and heart failure, and others. Muscle atrophy is defined by changes in the muscles, consisting in shrinkage of myofibers, changes in the types of fiber and myosin isoforms, and a net loss of cytoplasm, organelles and overall a protein loss. Although in the literature there are extensive studies in a range of animal models, the paucity of human data is a reality. This chapter is focused on various aspects of muscle wasting and describes the transitions of myofiber types during the progression of muscle atrophy in several pathological states. Clinical conditions associated with muscle atrophy have been grouped based on the fast-to-slow or slow-to-fast fiber-type shifts. We have also summarized the ultrastructural and histochemical features characteristic for muscle atrophy in clinical and experimental models for aging, cancer, diabetes and obesity, and heart failure and arrhythmia.

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Previous studies have demonstrated that endurance exercise training increases the level of heat shock proteins (HSPs) in skeletal muscles. However, little attention has been drawn to the effects of high intensity-short duration exercise, or sprint- interval training (SIT) on HSP72 level in rat skeletal muscles. This study performed to test the hypothesis that the SIT would induce the HSP72 in fast and slow skeletal muscles of rats. Young male Wistar rats (8 weeks old) were randomly assigned to a control (CON) or a SIT group (n = 8/group). Animals in the SIT group were trained (1 min/sprint, 6~10 sets/day and 5~6 days/week) on a treadmill for 9 weeks. After the training period, HSP72 levels in the plantaris (fast) and soleus (slow) muscles were analyzed by Western blotting method. Enzyme activities (hexokinase, phosphofructokinase and citrate synthase) and histochemical properties (muscle fiber type compositions and cross sectional area) in both muscles were also determined. The SIT resulted in significantly (p < 0.05) higher levels of HSP72 in both the plantaris and soleus muscles compared to the CON group, with the plantaris producing a greater HSP72 increase than the soleus (plantaris; 550 ± 116%, soleus; 26 ± 8%, p < 0.05). Further, there were bioenergetic improvements, fast-to-slow shift of muscle fiber composition and hypertrophy in the type IIA fiber only in the plantaris muscle. These findings indicate that the SIT program increases HSP72 level of the rat hindlimb muscles, and the SIT-induced accumulation of HSP72 differs between fast and slow muscles. Key PointsThere is no study about the effects of high intensity but short duration exercise, or sprint-interval training (SIT) on heat shock protein 72 (HSP72) level in skeletal muscles.The SIT program (≤ 10 min·day(-1)) accumulated HSP72 in rat skeletal muscles.The SIT-induced accumulation of HSP72 in the plantaris (fast) muscle was drastic compared to the soleus (slow) muscle and accompanied with the improvements of enzyme activities, fast-to-slow shift within fast muscle fiber type and muscle hypertrophy.