Does insulin-like growth factor 1 genotype influence muscle power response to strength training in older men and women?

The CA-repeat polymorphism in the insulin-like growth factor 1 (IGF1) gene promoter region has been associated with strength and circulating IGF-I protein levels. The purpose of the study was to determine if the IGF1 CA-repeat polymorphism influences muscle power at baseline and in response to ST in older adults. Knee extensor peak power (PP) was measured at 50, 60, and 70% of 1-RM strength before and after 10 weeks of unilateral knee extensor ST in older adults, aged 50-85 years, to determine the changes in absolute and relative PP with ST. Subjects (N = 114) were genotyped for the IGF1 CA-repeat polymorphism and grouped as homozygous for the 192 allele, heterozygous, or non-carriers of the 192 allele. The 192 homozygotes had significantly lower baseline PP at 50, 60, and 70% of 1-RM strength than the non-carriers when age, sex, and baseline fat-free mass were covaried (all P < 0.05). This same relationship was observed when the highest PP within these ranges was compared (e.g., 317.6 ± 13.5 for 192 homozygotes and 380.2 ± 16.3 for non-carriers of the 192 allele, P < 0.05). Both absolute and relative PP increased significantly with ST in all genotype groups as expected, but there were no significant relationships among IGF1 genotypes and any of the PP changes. Despite a significant relationship between IGF1 genotype and knee extensor peak power at baseline, IGF1 genotype does not appear to influence changes in knee extensor peak power with ST.

Influence of promoter region variants of insulin-like growth factor pathway genes on the strength-training response of muscle phenotypes in older adults.

To examine the influence of insulin-like growth factor (IGF) pathway gene polymorphisms on muscle mass and strength responses to strength training (ST), we studied 128 White and Black men and women before and after a 10-wk single-leg knee extension ST program. One-repetition maximum strength, muscle volume (MV) via computed tomography, and muscle quality (MQ) were assessed at baseline and after 10 wk of ST. There was a significant combined IGF1 cytosine adenine (CA) repeat gene effect, which included both the IGF1 CA repeat main effect and IGF1 CA repeat x PPP3R1 insertion-deletion (I/D) gene x gene interaction effect, on the changes in strength (P < 0.01) and MQ (P < 0.05) with ST. There was a trend for a significant gene x gene interaction between IGF1 CA repeat and PPP3R1 I/D for changes in strength (P = 0.07) and MQ (P = 0.06) with ST. The influence of the PPP3R1 A-202C gene polymorphism on change in MV with ST approached significance (P = 0.06). The IGF1 CA repeat polymorphism had a significant influence on the change in strength and MV combined with ST (P < 0.05), whereas the influence of the PPP3R1 I/D polymorphism approached significance (P = 0.08). There were no associations between the IGFBP3 A-202C gene polymorphism and the muscle phenotypic responses to ST. These data suggest that two of the three IGF pathway gene polymorphisms identified in this study influence muscle phenotypic responses to ST in both black and white older men and women.

Adrenergic receptor genotype influence on midthigh intermuscular fat response to strength training in middle-aged and older adults.

BACKGROUND: There is little information regarding the effects of strength training on intermuscular fat (IMF). This study examines changes in IMF in response to strength training in carriers of the adrenergic receptor (ADR) beta2Glu27 polymorphism versus noncarriers and between carriers of ADRalpha2b Glu(9) polymorphism versus noncarriers. METHODS: Midthigh IMF and muscle area were measured by computed tomography (CT) before and after 10 weeks of single-leg strength training in healthy, sedentary middle-aged and older (50-83 years) men (n = 46) and women (n = 52) in both their trained and untrained (control) legs. RESULTS: The strength training program resulted in a substantial increase in one-repetition maximum strength (p <.001) and muscle area (p <.001), but no significant changes in IMF in the whole group. However, IMF was significantly reduced with strength training in participants carrying ADRbeta2 Glu27 (-2. 3 +/- 1.0 cm(2), p =.028), but no significant change was observed with ADRbeta2 Glu27 noncarriers. The decrease in IMF in ADRalpha2b Glu(9) carriers (-1.9 +/- 1.0 cm(2), p =.066) was significantly different (-2.9 +/- 1.5 cm(2), p =.043) from a nonsignificant increase in ADRalpha2b Glu(9) noncarriers. ADRbeta2 Glu27 carriers who also carried ADRalpha2b Glu(9) significantly lost IMF with strength training (-3.8 +/- 1.5 cm(2), p =.018). CONCLUSION: ADR genotype influences IMF response to strength training.

Alpha-actinin-3 (ACTN3) R577X polymorphism influences knee extensor peak power response to strength training in older men and women.

BACKGROUND: The alpha-actinin-3 (ACTN3) R577X polymorphism has been associated with muscle power performance in cross-sectional studies. METHODS: We examined baseline knee extensor concentric peak power (PP) and PP change with approximately 10 weeks of unilateral knee extensor strength training (ST) using air-powered resistance machines in 71 older men (65 [standard deviation = 8] years) and 86 older women (64 [standard deviation = 9] years). RESULTS: At baseline in women, the XX genotype group had an absolute (same resistance) PP that was higher than the RR (p =.005) and RX genotype groups (p =.02). The women XX group also had a relative (70% of one-repetition maximum [1-RM]) PP that was higher than that in the RR (p =.002) and RX groups (p =.008). No differences in baseline absolute or relative PP were observed between ACTN3 genotype groups in men. In men, absolute PP change with ST in the RR (n = 16) group approached a significantly higher value than in the XX group (n = 9; p =.07). In women, relative PP change with ST in the RR group (n = 16) was higher than in the XX group (n = 17; p =.02). CONCLUSIONS: The results indicate that the ACTN3 R577X polymorphism influences the response of quadriceps muscle power to ST in older adults.

AMPD1 gene polymorphism and the vasodilatory response to ischemia.

Peripheral vasculature resistance can play an important role in affecting blood pressure and the development of cardiovascular disease. A better understanding of the genes that encode vasodilators, such as adenosine, will provide insight into the mechanisms underlying cardiovascular disease. We tested whether the adenosine monophosphate deaminase-1 (AMPD1) C34T gene polymorphism was associated with the vasodilatory response to ischemia in Caucasian females aged 18-35 years. Blood samples (n = 58) were analyzed for the C34T variant and resulted in the following genotype groups: CC (n = 45) and CT (n = 13). Mean blood pressure (MBP), heart rate, and forearm blood flow (FBF) measured by venous occlusion plethysmography were measured at baseline and at 1 (peak FBF), 2 and 3 min of vasodilation during reactive hyperemia following 5 min of arm ischemia. To control for interindividual variability in baseline FBF and forearm vascular resistance (FVR) the percent change in FBF and FVR were calculated for each min. The percent decrease in FVR was significantly greater in the CT compared to the CC genotype group (-40+/-4% vs. -24+/-3%, P = 0.01) during the 2nd min of reactive hyperemia. The percent increase in FBF tended to be greater in the CT compared to the CC genotype group (+69+/-9% vs. +42+/-9%, P = 0.07) during the 2nd min of reactive hyperemia after adjustment for percent body fat. Consistent with previous findings of increased production of adenosine during exercise in individuals carrying a T allele, our findings suggest that the AMPD1 C34T polymorphism is associated with vasodilatory response to ischemia in the peripheral vasculature because individuals with the T allele had a greater vasodilatory response to ischemia.

Muscle-power quality: does sex or race affect movement velocity in older adults?

To determine sex and race differences in muscle power per unit of muscle contraction, knee-extensor muscle power normalized for knee-extensor muscle volume was measured in 79 middle-aged and older adults (30 men and 49 women, age range 50-85 years). Results revealed that women displayed a 38% faster peak movement velocity than men and African Americans had a 14% lower peak movement velocity than Whites of a similar age when expressed per unit of involved muscle (p < .001). As expected, men exhibited greater knee-extensor strength and peak power per unit of muscle than women, but women had a faster knee- extension movement velocity per unit of muscle than men at the same relative strength level. Moreover, African Americans had greater knee-extensor muscle volume than Whites but exhibited lower knee-extensor strength and lower movement velocity per unit of muscle when tested at the same relative strength levels.

Effects of moderate-velocity strength training on peak muscle power and movement velocity: do women respond differently than men?

The effects of a 10-wk unilateral knee extension strength training (ST) program on peak power (PP) and peak movement velocity (PV), at given absolute (force load) and relative (same % of 1 repetition maximum) resistances (loads), were examined in 30 older men [64 yr (7 SD)] and 32 older women [62 yr (6 SD)]. PP increased significantly in both men and women at the same absolute (P < 0.001) and relative loads (P < 0.01) with ST. Men had a significantly greater increase in relative PP than women with ST at 60% (P < 0.01) and 70% (P < 0.001) of 1 repetition maximum when covarying for baseline differences and age. However, when each subject was tested at the same absolute load and when PP was normalized for the muscle volume of the trained knee extensors (i.e., absolute muscle power quality), women increased by 9% (P < 0.05), whereas men did not change. Both men and women increased their absolute PV (P < 0.001) but decreased their relative PV significantly with ST (P < 0.05). However, when baseline values and age were covaried, women had significantly less of a decrease in relative PV quality with ST than men (P < 0.01), although the difference was small. These normalized data suggest that ST-induced increases in PP depend on muscular hypertrophy in men, but not in women, providing further support for the hypothesis developed from our previous report (Ivey FM, Tracy BL, Lemmer JT, NessAiver M, Metter EJ, Fozard JL and Hurley BF. J Gerontol A Biol Sci Med Sci 55: B152-B157, 2000) that improvements in muscle function with ST result from nonmuscle mass adaptations to a greater extent in women than men.