Higbie, Elizabeth J., Kirk J. Cureton, Gordon L. Warren III, and Barry M. Prior. Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation.J. Appl. Physiol. 81(5): 2173–2181, 1996.—We compared the effects of concentric (Con) and eccentric (Ecc) isokinetic training on quadriceps muscle strength, cross-sectional area, and neural activation. Women (age 20.0 ± 0.5 yr) randomly assigned to Con training (CTG;n = 16), Ecc training (ETG;n = 19), and control (CG;n = 19) groups were tested before and after 10 wk of unilateral Con or Ecc knee-extension training. Average torque measured during Con and Ecc maximal voluntary knee extensions increased 18.4 and 12.8% for CTG, 6.8 and 36.2% for ETG, and 4.7 and −1.7% for CG, respectively. Increases by CTG and ETG were greater than for CG (P < 0.05). For CTG, the increase was greater when measured with Con than with Ecc testing. For ETG, the increase was greater when measured with Ecc than with Con testing. The increase by ETG with Ecc testing was greater than the increase by CTG with Con testing. Corresponding changes in the integrated voltage from an electromyogram measured during strength testing were 21.7 and 20.0% for CTG, 7.1 and 16.7% for ETG, and −8.0 and −9.1% for CG. Quadriceps cross-sectional area measured by magnetic resonance imaging (sum of 7 slices) increased more in ETG (6.6%) than in CTG (5.0%) (P< 0.05). We conclude that Ecc is more effective than Con isokinetic training for developing strength in Ecc isokinetic muscle actions and that Con is more effective than Ecc isokinetic training for developing strength in Con isokinetic muscle actions. Gains in strength consequent to Con and Ecc training are highly dependent on the muscle action used for training and testing. Muscle hypertrophy and neural adaptations contribute to strength increases consequent to both Con and Ecc training.

Purpose: Our objective was to perform a systematic review and meta-analysis of the research literature assessing the effect of caffeine ingestion on maximal voluntary contraction (MVC) strength and muscular endurance. Methods: Thirty-four relevant studies between 1939 and 2008 were included in the meta-analyses of caffeine's effects on MVC strength (n = 27 studies) and muscular endurance (n = 23 studies). Effect sizes (ES) were calculated as the standardized mean difference and meta-analyses were completed using a random-effects model. Results: Overall, caffeine ingestion was found to result in a small beneficial effect on MVC strength (overall ES = 0.19, P = 0.0003). However, caffeine appears to improve MVC strength primarily in the knee extensors (i.e., by ∼7%, ES = 0.37) and not in other muscle groups such as the forearm or the knee flexors. In an attempt to offer a physiological mechanism behind caffeine's ability to improve MVC strength, a meta-analysis was run on ES from nine studies that measured percent muscle activation during MVC in trials comparing caffeine versus placebo; the overall ES (0.67) was highly significant (P = 0.00008) and of moderate to large size, thus implicating an effect of caffeine on the CNS. Caffeine ingestion was also found to exert a small beneficial effect on muscular endurance (overall ES = 0.28, P = 0.00005). However, it appears caffeine improves muscular endurance only when it is assessed using open (i.e., by ∼18%, ES = 0.37) and not fixed end point tests. Conclusions: Overall, caffeine ingestion improves MVC strength and muscular endurance. The effect on strength appears exclusively in the knee extensors, and the effect on muscular endurance appears only detectable with open end point tests.

The study evaluates the influence of monocytes/macrophages in the mechanisms of skeletal muscle injury using a mouse model and selective depletion of peripheral monocyte with systemic injections of liposomal clodronate (dichloromethylene bisphosphonate). This pharmacological treatment has been demonstrated to induce specific apoptotic death in monocytes and phagocytic macrophages. In the current studies, the liposomal clodronate injections resulted in a marked attenuation of the peak inflammatory response in the freeze-injured muscle in the first three days after injury. The effect was accompanied by a transient reduction (at day 1 or 3 postinjury) of the expression of several genes coding for inflammatory, as well as growth-related mediators, including TNF, monocyte chemoattractant protein (MCP)-1, thioredoxin, high-mobility group AT-hook 1, insulin-like growth factor-binding protein (IGFBP), and IGF-1. In contrast, the expression of major myogenic factors (i.e., MyoD and myogenin) directly involved in the activation/proliferation and differentiation of muscle precursor cells was not altered by the clodronate liposome treatment. The repair process in the injured muscle of clodronate liposome-treated mice was characterized by prolonged clearance of necrotic myofibers and a tendency for increased muscle fat accumulation at day 9 and 14 postinjury, respectively. In conclusion, a significant reduction of the initial monocyte/macrophage influx into the injured muscle is associated with not improved, but moderately impaired, repair processes after skeletal muscle injury.

The degenerative and regenerative roles of tumor necrosis factor α (TNF‐α), a pro‐inflammatory cytokine with pleiotropic functions, were investigated by using TNF receptor 1 and 2 double knockout (TNFR‐DKO) and TNF‐α antibody neutralized mice following traumatic freeze injury to the tibialis anterior muscle. In wild‐type control mice, TNF‐α mRNA transcripts and protein increased following injury and gradually returned to control (uninjured) levels by 13 days. A reduction in MyoD mRNA expression occurred in TNF–α‐deficient mice, although there were no visible differences in MyoD immunostaining or histological characteristics in regenerating muscles. At 5 days post‐injury, the reductions in isometric strength in TNFR‐DKO and TNF–α‐depleted mice did not differ from that of wild‐type mice but by 13 days after injury, the TNFR‐DKO and TNF–αdepleted mice exhibited strength deficits twice that of wild‐type mice (i.e., 27–31% vs 13%). Muscle injury was also accompanied by increased expression of interleukin‐6 (IL‐6), but IL–6‐deficient mice demonstrated MyoD expression and recovery of isometric strength similar to that of wild‐type mice. These data indicate that TNF‐α is involved in the recovery of muscle function after traumatic muscle injury, and this effect might be associated with modulation of muscle regulatory genes, including MyoD.