The effects of ageing and exercise on skeletal muscle structure and function

Musculoskeletal ageing is associated with profound morphological and functional changes that increase fall risk and disease incidence and is characterised by age-related reductions in motor unit number and atrophy of muscle fibres, particularly type II fibres. Decrements in functional strength and power are relatively modest until the 6th decade, after which the rate of loss exponentially accelerates, particularly beyond the 8th decade of life. Physical activity is a therapeutic modality that can significantly attenuate age-related decline. The underlying signature of ageing, as manifested by perturbed redox homeostasis, leads to a blunting of acute and chronic redox regulated exercise adaptations. Impaired redox regulated exercise adaptations are mechanistically related to altered exercise-induced reactive oxygen and nitrogen species generation and a resultant failure to properly activate redox regulated signaling cascades. Despite the aforementioned specific impairment in redox signaling, exercise induces a plethora of beneficial effects, irrespective of age. There is, therefore, strong evidence for promoting regular physical exercise, especially progressive resistance training as a lifelong habitual practice.

Role of active and passive recovery in adaptations to high intensity training

It has been established that Wingate-based high-intensity training (HIT) consisting of 4 to 6 x 30-s all-out sprints interspersed with 4-min recovery is an effective training paradigm. Despite the increased utilisation of Wingate-based HIT to bring about training adaptations, the majority of previous studies have been conducted over a relatively short timeframe (2 to 6 weeks). However, activity during recovery period, intervention duration or sprint length have been overlooked. In study 1, the dose response of recovery intensity on performance during typical Wingate-based HIT (4 x 30-s cycle all-out sprints separated by 4-min recovery) was examined and active recovery (cycling at 20 to 40% of V̇O2peak) has been shown to improve sprint performance with successive sprints by 6 to 12% compared to passive recovery (remained still), while increasing aerobic contribution to sprint performance by ~15%. In the following study, 5 to 7% greater endurance performance adaptations were achieved with active recovery (40%V̇O2peak) following 2 weeks of Wingate-based HIT. In the final study, shorter sprint protocol (4 to 6 x 15-s sprints interspersed with 2 min of recovery) has been shown to be as effective as typical 30-s Wingate-based HIT in improving cardiorespiratory function and endurance performance over 9 weeks with the improvements in V̇O2peak being completed within 3 weeks, whereas exercise capacity (time to exhaustion) being increased throughout 9 weeks. In conclusion, the studies demonstrate that active recovery at 40% V̇O2peak significantly enhances endurance adaptations to HIT. Further, the duration of the sprint does not seem to be a driving factor in the magnitude of change with 15 sec sprints providing similar adaptations to 30 sec sprints. Taken together, this suggests that the arrangement of recovery mode should be considered to ensure maximal adaptation to HIT, and the practicality of the training would be enhanced via the reduction in sprint duration without diminishing overall training adaptations.