Essential Amino Acids and Exercise Tolerance in Elderly Muscle-Depleted Subjects with Chronic Diseases: A Rehabilitation without Rehabilitation?

Table 3

EAA physiological activities and histological-biochemical findings from in vivo and human studies following chronic EAA supplementation, explaining the EAA mechanisms in improving exercise intolerance in CHF/COPD.

Mechanisms and measures in CHF/COPD	Physiological activities	Findings from experimental and human studies
		Biochemistry	Histology
Increased aerobic metabolism; WT; Steps/day; VO2 peak; Time VO2 peak to baseline; Resting plasma lactate levels	EAAs used as fuel for TCA cycle	↑ ATP production and ↑ cell ATP availability [15]; Shift of ventricular MHC from 𝛽 to 𝛼 type [16]; ↑ COX and NADH^+ activities [16]; ↑ SOD [17]	↑ Mitochondria number: +310% skeletal muscle; +40% myocardium [18]; ↑ 28% increased mitochondria volume [18]; ↑ Mitochondrial biogenesis and sirtuin 1 expression in cardiac and skeletal muscle [19]; ↑ Vsar/Vtot fiber ratio [20]
Improved nutritional status; FFM; Body weight; Muscle strength; Serum albumin levels	↑ Protein synthesis [21–23]; ↓ Proteolysis [24]; ↑ IGF-1 expression [25]	↓ TNF alpha/IGF 1 ratio [14]	↑ 40% myofibrils of quadriceps muscle [18]; ↓ Muscle fibrosis [18]; ↑ Type II A fibers [20]; ↑ Cross-sectional area of skeletal muscle fibers [20]
Reduced insulin resistance	Upregulated insulin-receptor synthesis and its autophosphorylation [14]	↓ HOMA index [14]; ↓ Fasting insulin levels [14]; ↓ Fasting blood glucose [14]; ↓ TNF alpha/IGF 1 ratio [14]

WT: walking test; VO_2: oxygen consumption; FFM: fat free mass; TCA: tricarboxylic cycle acid; ATP: adenosine triphosphate; COX: cytochrome oxidase; NADH: nicotinamide adenine dehydrogenase; SOD: superoxide dismutase; IGF-1: insulin-like growth factor-1; TNF: tumor necrosis factor; Vsar/Vtot: volume of sarcomeres/total volume ratio.