Continuing my summary of Jonathan Sullivan's "The Year in Strength Science, 2013" with Part II on Exercise Physiology. (full text)
(1) "Nilwik et al [18] present data suggesting that the decline in muscle mass with aging is almost entirely due to a reduction in Type II muscle fiber size – but not number. . . . it’s a happy thought, because making atrophic Type II fibers larger with training is a rather more tractable prospect than replacing lost fibers…which probably doesn’t happen to any clinically relevant degree." (pp. 9-10)
(2) "In a related study, Verdijk [19] et al looked at satellite cells [a type of stem cell specific to muscle tissue] in human muscle in 165 subjects ranging in age from < 18 to 86 years old. . . . As in the Nilwik, older subjects demonstrated Type II fiber atrophy. This was accompanied by a decrease in Type II fiber-associated satellite cells. Twelve weeks of strength training increased Type II fiber muscle size and satellite cell content. These two important papers, taken together, underscore the power of resistance exercise in older populations, the relative susceptibility of Type II fibers (the strong/powerful fibers) to aging and atrophy, and the responsiveness of these fibers to even very brief periods of strength training." (p. 10)
(3) "Mitchell et al [21] continue the attack on a rapidly eroding model of muscle hypertrophy in which circulating trophic factors stimulate muscle growth. Like other investigators, they found little correlation between circulating hormones (testosterone, IGF-1) and muscle protein accretion. In line with a growing consensus, they conclude that muscle responses to training are dominated by paracrine and autocrine effects – within the tissue itself, rather than from factors released into the circulation. I think that’s probably right, although this paper doesn’t prove it. But I also think it glosses over an important set of questions. Circulating trophic factors may very well not be directly responsible for muscle protein accretion after exercise. But circulating levels of those factors are nevertheless increased by resistance exercise. Why? And to what purpose?" (p. 11)
(4) "Hacket and Chow present us with a systematic review of the literature on the Valsalva maneuver [29]. . . . For me, however, one of the most important findings of this paper is that
the literature strongly indicates that the Valsalva is a reflexive and virtually unavoidable response to lifting loads at high intensity. And this underscores a point I made in my own review: prohibition of the Valsalva is tantamount to a prohibition of heavy lifting itself." (pp. 14-15)
(5) "Luo et al [31] present data in the rat supporting pro-autophagic and anti-apoptotic effects of chronic resistance training on aging muscle. . . . Apoptosis, as I’ve discussed elsewhere, is a regulated form of “cell suicide.”. . . This paper, with all its limitations, is a data point in favor of the view that resistance training down-regulates muscle apoptosis."
(1) "Nilwik et al [18] present data suggesting that the decline in muscle mass with aging is almost entirely due to a reduction in Type II muscle fiber size – but not number. . . . it’s a happy thought, because making atrophic Type II fibers larger with training is a rather more tractable prospect than replacing lost fibers…which probably doesn’t happen to any clinically relevant degree." (pp. 9-10)
(2) "In a related study, Verdijk [19] et al looked at satellite cells [a type of stem cell specific to muscle tissue] in human muscle in 165 subjects ranging in age from < 18 to 86 years old. . . . As in the Nilwik, older subjects demonstrated Type II fiber atrophy. This was accompanied by a decrease in Type II fiber-associated satellite cells. Twelve weeks of strength training increased Type II fiber muscle size and satellite cell content. These two important papers, taken together, underscore the power of resistance exercise in older populations, the relative susceptibility of Type II fibers (the strong/powerful fibers) to aging and atrophy, and the responsiveness of these fibers to even very brief periods of strength training." (p. 10)
(3) "Mitchell et al [21] continue the attack on a rapidly eroding model of muscle hypertrophy in which circulating trophic factors stimulate muscle growth. Like other investigators, they found little correlation between circulating hormones (testosterone, IGF-1) and muscle protein accretion. In line with a growing consensus, they conclude that muscle responses to training are dominated by paracrine and autocrine effects – within the tissue itself, rather than from factors released into the circulation. I think that’s probably right, although this paper doesn’t prove it. But I also think it glosses over an important set of questions. Circulating trophic factors may very well not be directly responsible for muscle protein accretion after exercise. But circulating levels of those factors are nevertheless increased by resistance exercise. Why? And to what purpose?" (p. 11)
(4) "Hacket and Chow present us with a systematic review of the literature on the Valsalva maneuver [29]. . . . For me, however, one of the most important findings of this paper is that
the literature strongly indicates that the Valsalva is a reflexive and virtually unavoidable response to lifting loads at high intensity. And this underscores a point I made in my own review: prohibition of the Valsalva is tantamount to a prohibition of heavy lifting itself." (pp. 14-15)
(5) "Luo et al [31] present data in the rat supporting pro-autophagic and anti-apoptotic effects of chronic resistance training on aging muscle. . . . Apoptosis, as I’ve discussed elsewhere, is a regulated form of “cell suicide.”. . . This paper, with all its limitations, is a data point in favor of the view that resistance training down-regulates muscle apoptosis."
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