The power output at VO_2max, when normalised for body mass, is an index which considers both the power output of recruited skeletal muscle and the maximal aerobic capacity. Therefore, for cyclists, this is a measure of the functional capacity of skeletal muscle at VO_2max. This study reported an age-associated decrease in relative power at VO_2max in males but not in females, thus suggesting that the female cohort maintained peak aerobic power throughout the age range. Although speculative, this may suggest that peak aerobic power may be maintained if there are no age-associated changes in maximal oxygen pulse and HR_max, both findings consistent with current data.

A sub-maximal sustainable power (for example the power output at the onset of the accumulation of blood lactate) may represent a measure of muscle performance potentially unaffected by the age-associated declines in maximal cardiac output, reduced peak muscle blood flow, and decreases in oxygen extraction. The current study reported that power output at [La^-]_4mmol, when normalised for body mass, declined with age in both males and females. The near parallel age-associated declines in peak aerobic power and power at [La^-]_4mmol in males may suggest a common mechanism, for example, a decrease in peripheral oxygen uptake (indirectly supported by the age-associated decline in maximum oxygen pulse), or a decrease in cardiac output (indirectly supported by the age-associated decline in HR_max). The apparent divergence of the regression lines for the female data should be treated with caution, however, the age-associated decline in power at [La^-]_4mmol in the females may suggest age- associated changes in the kinetics of lactate production and/or clearance. Further work on the mechanisms responsible for gender specific changes in sub-maximal and peak aerobic power is required.

An age-associated decrease in muscle mass and/or changes in the expression of the myosin heavy chain (MHC) isoforms in the recruited motor unit pool (Doherty, 2003; Goldspink, 2005) may contribute to the decline in power with age. Farina et al. (2007) reported a correlation between % MHC type 1 isoform with power at the lactate threshold and at VO_2max in trained subjects (aged 25 ± 4 years, VO_2max 52.5 ml·kg^-1·min^-1), whereas Mattern et al., 2003 found no differences between young and old subjects in the MHC isoforms expressed in skeletal muscle. However, Mattern et al., 2003 did show that age and MHC type 1 combined to account for 58% of the variance in power output at the maximum sustainable stable blood lactate concentration when expressed as a % of maximal aerobic capacity. A lower power output at the maximum sustainable stable blood lactate concentration in older, trained endurance athletes, has been reported (Mattern et al., 2003) where subjects (n = 9, VO_2max 67.7 ml·kg^-1·min^-1) aged 25 years produced 3.5 W·kg^-1, and subjects (n = 9, VO_2max 47.0 ml·kg^-1·min^-1) aged 65 years produced 2.2 W·kg^-1. The present study predicted power at [La^-]_4mmol when aged 25 to be 3.41 W·kg^-1, and when aged 65 to be 2.41 W·kg^-1.

There is certainly some variability in the age- associated decline in VO_2max in trained subjects, whether approximate rates are derived from longitudinal or cross-sectional studies, and both experimental designs have limitations. We have included all ages into gender-specific regression models - consistent with previous reports (Fitzgerald et al., 1997; Wilson and Tanaka, 2000), and acknowledge that a selection bias, whereby the oldest athletes are selected from a decreasing pool of available subjects (Katzel et al., 2001) exists in the current data. The cross-sectional age-associated decrease in VO_2max reported in the present study was lower than that reported by Tanaka et al., 1997 for endurance athletes, but higher than that reported by Katzel et al., 2001 in their cross-sectional study. Katzel et al., 2001 reported higher values for the rate of decline in their longitudinal study, and Marcell et al., 2003 reported a rate of 1 ml·kg^-1·min^-1·year^-1 in trained men and women aged 40 - 60 years over an approximate 6 year period. It has been reported that longitudinal studies generally report higher rates of decline in VO_2max with age (Eskurza et al., 2002; Katzel et al., 2001), and Stathokostas et al., 2004 reported that the longitudinal rate of decline in men was higher than that reported in a cross- section of their original sample population. Pimental et al. (2003), when stratifying for age, reported that endurance trained subjects showed declines of 0.2 ml kg^-1min^-1year^-1 when aged 20-50 years, and this increased to 0.89 ml·kg^-1·min^-1·year^-1 when aged 50-75 years. We acknowledge that the age range used in the current study does not include 'old' athletes, and the limited sample size prevents stratification by age.

An age-associated decline in HR_max has been previously reported (Fitzgerald et al., 1997; Tanaka et al., 1997; Pimentel et al., 2003;Wilson and Tanaka, 2000), although in the present study there was no obvious trend in HR_max for females and only a weak age- associated decrease in male HR_max. The lack of an age-associated decline in HR_max in the present study may be a result of fatigue, given that the VO_2max protocol was at the end of the exercise period. However, we were satisfied that all subjects reached VO_2max using this protocol. Decreases (Rogers et al., 1990; Fleg et al., 2005) or no changes (Ogawa et al., 1992; Stathokostas et al., 2004) in maximal oxygen pulse with age have been previously reported without consistent directional changes in HR_max.

Differences in the rate at which VO_2max declined with advancing age has been attributed to gender-specific changes in components of the cardiovascular system (Weiss et al., 2006). The current study reported no correlation between age and maximum oxygen pulse in females, but a significant negative correlation in males, thus further supporting gender-specific differences in the rate of decline in cardiovascular performance. However, it should be noted that the small sample size and lack of old (60 years +) subjects (particularly females) used in the current study, make such statements speculative.

Linear equations have been used to express the maximal aerobic capacity of skeletal muscle as a function of muscle mass where Proctor and Joyner, 1997 reported the same gradient for young compared to old muscle. This indicated that for a given change in muscle mass, the proportional change in aerobic capacity of young and old muscle was the same. The authors concluded that it was unlikely that skeletal muscle oxidative capacity or capillarisation was responsible for the age-associated reduction in aerobic capacity per Kilogramme muscle in trained older subjects (Proctor and Joyner, 1997). Mattern et al., 2003 also reported no differences in the citrate synthase activity of skeletal muscle samples taken from young, middle aged, and older trained endurance athletes, thus supporting the conclusions of Proctor and Joyner, 1997. However, the ordinary least-squares model used by Rosen et al., 1998 suggested that 35% of the age-associated decline in VO_2max was due to a loss of fat free mass, accounting for approximately 8 ml min^-1·year^-1.

In the current study, we chose to use the same testing protocol for all ages and both genders - a decision based on the selection of the subjects (all well trained and in regular competition), and following medical screening. Variations in training regimes are likely to occur with aging (Spirduso et al., 2005), although subjects in the current study all participated in at least 2 high intensity training sessions each week - in most cases this was in addition to a weekly competitive event. Our experiences in recruiting trained athletes across a wide age-range is that older subjects do not have a lower training volume in comparison to their younger counterparts, however, we acknowledge that medical conditions which impact on the ability to perform high-intensity exercise may define the appropriate testing protocols suitable for older subjects (Huggett et al., 2005).