Novel, high-intensity exercise prescription improves muscle mass, mitochondrial function, and physical capacity in individuals with Parkinson's disease

Abstract

We conducted, in persons with Parkinson's disease (PD), a thorough assessment of neuromotor function and performance in conjunction with phenotypic analyses of skeletal muscle tissue, and further tested the adaptability of PD muscle to high-intensity exercise training. Fifteen participants with PD (Hoehn and Yahr stage 2-3) completed 16 wk of high-intensity exercise training designed to simultaneously challenge strength, power, endurance, balance, and mobility function. Skeletal muscle adaptations (P < 0.05) to exercise training in PD included myofiber hypertrophy (type I: +14%, type II: +36%), shift to less fatigable myofiber type profile, and increased mitochondrial complex activity in both subsarcolemmal and intermyofibrillar fractions (I: +45-56%, IV: +39-54%). These adaptations were accompanied by a host of functional and clinical improvements (P < 0.05): total body strength (+30-56%); leg power (+42%); single leg balance (+34%); sit-to-stand motor unit activation requirement (-30%); 6-min walk (+43 m), Parkinson's Disease Quality of Life Scale (PDQ-39, -7.8pts); Unified Parkinson's Disease Rating Scale (UPDRS) total (-5.7 pts) and motor (-2.7 pts); and fatigue severity (-17%). Additionally, PD subjects in the pretraining state were compared with a group of matched, non-PD controls (CON; did not exercise). A combined assessment of muscle tissue phenotype and neuromuscular function revealed a higher distribution and larger cross-sectional area of type I myofibers and greater type II myofiber size heterogeneity in PD vs. CON (P < 0.05). In conclusion, persons with moderately advanced PD adapt to high-intensity exercise training with favorable changes in skeletal muscle at the cellular and subcellular levels that are associated with improvements in motor function, physical capacity, and fatigue perception.

Keywords: Parkinson's disease; high-intensity exercise; mitochondria; muscle hypertrophy; resistance training.

Fig. 1.

Skeletal myofiber morphometry. Effects of Parkinson's disease (PD) and high-intensity exercise training on type I (A) and type II (B) skeletal myofiber size, and the relative distribution of myofibers by type (I, IIa, IIx) (C). Representative immunohistological images are shown in D (type I, copper; type IIa, green; type IIx, dark/negative). CSA, cross-sectional area; PD, Parkinson's disease; CON, non-PD, untrained, matched controls. *Different from pretraining, P < 0.05. †Different from control, P < 0.05. Values are means + SE.

Fig. 2.

Skeletal muscle mitochondrial function. Effects of Parkinson's disease (PD) and high-intensity exercise training on the activities of skeletal muscle mitochondrial complex I (A and B) and complex IV (C and D) in intermyofibrillar (IMF) (A and C) and subsarcolemmal (SS) (B and D) fractions of mitochondria. *Different from pretraining, P < 0.05. Values are means + SE.

Fig. 3.

Neuromuscular performance. Effects of Parkinson's disease (PD) and high-intensity exercise training on one-repetition maximum (1RM) knee extension strength (A); peak knee extension power working against a resistance equal to 45% of current 1RM (B); specific strength (leg press 1RM/kg thigh lean mass) (C); motor unit activation (relative to maximum) during the concentric phase of standing from a seated position (D); fatigability during a 20-repetition maximum speed sit-to-stand test (E); and fatigability during electrically elicited isometric contractions (90 repeat 1 s contractions)(F). *Different from week 0, P < 0.05. #Different from week 8, P < 0.05. “f” indicates significant fatigue (final power during repetitions 19–20 different from peak power during repetitions 1–5), P < 0.05. Values are means ± SE.