Biology subjects

Patterson, M. A.

Publications and source records attributed to Patterson, M. A..

3 recordsLinked to original sources

bioRxiv2024

Residual force enhancement is not altered while force depression is amplified at the cellular level in old age

Residual force enhancement (rFE) and residual force depression (rFD) are history-dependent properties of muscle which refer to increased and decreased isometric force following a lengthening or shortening contraction, respectively. The history-dependence of force is greater in older than younger adults when assessed at the joint level. However, it is unclear whether this amplification of the history-dependence of force in old age is owing to cellular mechanisms or a consequence of age-related remodeling of muscle architecture. Single muscle fibres from the psoas major of old and young F344BN rats were dissected and chemically permeabilized. Single muscle fibres were mounted between a force transducer and length controller, then maximally activated (pCa 4.5). To assess rFD, fibers were actively shortened from 3.1 to 2.5{micro}m at both a slow (0.15Lo/s) and fast (0.6Lo/s) speed, with a fixed-end isometric reference contraction at 2.5{micro}m. To assess rFE, fibers were activated and stretched at 0.3Lo/s from a sarcomere length of 2.2 to 2.5{micro}m, and 2.7 to 3.0{micro}m, and compared to fixed-end isometric reference contractions at 2.5 and 3.0{micro}m, respectively. Isometric force was {approx}19% lower in old as compared with young (p<0.001). Upon normalizing to fibre cross-sectional area, there was no age-related difference in specific force (p>0.05). rFD was {approx}33% greater in old as compared with young (p<0.05), while rFE did not differ between groups (p>0.05). rFD is amplified in old age at the cellular level, while rFE appears to be unchanged, thus previously reported age-related modification of rFE occurs upstream from the cellular level.

physiology↗

bioRxiv2024

Residual force enhancement decreases when scaling from the single muscle fibre to joint level in humans

Residual force enhancement (rFE), defined as increased isometric force following active lengthening compared to a fixed-end isometric contraction at the same muscle length and level of activation, is present across all scales of muscle. While rFE is always present at the cellular level, often rFE non-responders are observed during joint-level voluntary contractions. We compared rFE between the joint level and single fibre level (vastus lateralis biopsies) in 16 young males. In-vivo voluntary knee-extensor rFE was measured by comparing steady-state isometric torque between a stretch-hold (maximal activation at 150{degrees}, stretch to 70{degrees}, hold) and a fixed-end isometric contraction, with ultrasonographic recording of vastus lateralis fascicle length (FL). Fixed-end contractions were performed at 67.5{degrees}, 70{degrees}, 72.5{degrees}, and 75{degrees}; the joint angle that most closely matched FL of the stretch-hold contractions isometric steady-state was used to calculate rFE. The starting and ending FLs of the stretch-hold contraction were expressed as % optimal FL, determined via torque-angle relationship. In single fibre experiments, the starting and ending fibre lengths were matched relative to optimal length determined from in-vivo testing, yielding an average sarcomere excursion of [~]2.2-3.4{micro}m. There was a greater magnitude of rFE at the single fibre ([~]20%) than joint level ([~]5%) (P=0.004), with non-responders only observed at the joint level. By comparing rFE across scales within the same participants, we show the development of the rFE non-responder phenomenon is upstream of rFEs cellular mechanisms, with rFE only lost rather than gained when scaling from single fibres to the joint level.

physiology↗

bioRxiv2023

Age-related blunting of serial sarcomerogenesis and mechanical adaptations following 2 weeks of maximal eccentric resistance training

BackgroundDuring natural aging, muscles atrophy, which is partly accounted for by a loss of sarcomeres in series. Serial sarcomere number (SSN) is associated with aspects of muscle mechanical function including the force-length and force-velocity-power relationships; hence, the age-related loss of SSN contributes to declining performance. Training emphasizing muscle lengthening (eccentric) contractions increases SSN in young healthy rodents. However, the ability for eccentric training to increase SSN and improve mechanical function in old age is unknown. MethodsTen young (9 months) and 11 old (33 months) Fisher344/BN F1 rats completed 4 weeks of unilateral isokinetic eccentric plantar flexion training 3 days/week. Pre- and post-training, the plantar flexors were assessed for maximum tetanic torque (ankle angles of 70{degrees} and 90{degrees}), the torque-frequency relationship (stimulation frequencies of 1-100 Hz), the passive torque-angle relationship (ankle angles of 110-70{degrees}), and the torque-angular velocity-power relationship (isotonic loads of 10%-80% maximum). Following post-training testing, rats were sacrificed, and the soleus, lateral gastrocnemius (LG), and medial gastrocnemius (MG) were harvested for SSN assessment by measuring sarcomere lengths with laser diffraction, with the untrained leg used as a control. ResultsIn the untrained leg/pre-training, old rats had lower SSN in the soleus (-9%), LG (-7%), and MG (-14%), lower maximum torque (-27 to -42%), power (-63%), and shortening velocity (-35%), and greater passive torque (+62 to +191%) than young. Young rats showed increased SSN from the untrained to the trained soleus and MG. In contrast, old rats had no change in soleus SSN between legs and experienced SSN loss in the LG. Pre- to post-training, young rats saw modest improvements in isometric mechanical function, including a 13% increase in maximum torque at 90{degrees} and 4-11% increases in 10-60 Hz torque. Old rats, however, had reductions in maximum torque (-35%), shortening velocity (-46%), and power (-63%), and increased passive torque (+24 to +51%) from pre- to post-training. ConclusionsEccentric training induced serial sarcomerogenesis and improved mechanical function in young rats, while old rats exhibited dysfunctional remodeling that led to impairments in muscle mechanical performance following training.

physiology↗